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We read with interest the case report by Moore et al1 on the diaphragm weakness of two patients after anatomically distant surgery.
We are currently following a patient who had bilateral paralysis of the diaphragm after a nephrectomy for renal cancer. The patient, a 60 year old male non-smoker without any concomitant cardiac or lung disease, underwent surgery in August 2004 and immediately after the operation he complained of orthopnoea. Chest radiographs showed the elevation of both hemidiaphragms, which was not present preoperatively, along with a restrictive ventilatory defect detected by spirometry (TLC 61% predicted, VC 72% predicted, FEV1 67% predicted, FEV1/VC 70%). The diagnosis of bilateral paralysis was confirmed by electromyography and respiratory muscle strength assessment in October 2004. Because of a nocturnal oxygen desaturation, he started with nightly non-invasive ventilation. Up to now he has also undergone periodic courses of respiratory muscle training. In 2004 and 2005 he was checked regularly and an improvement in VC was found, but not in Pimax nor in TwPdi. Moreover, at the December 2005 check up the nocturnal oxygen desaturation had significantly improved and the patient had stopped the ventilation support.
Diaphragm paralysis is associated with renal cancer and is considered to be a paraneoplastic syndrome.2,3 In our patient, however, the temporal link between the surgical operation and paralysis is evident. Moreover, during the operation and after the perioperative period our patient did not undergo central venous cannulation, nor did he experience any electrolyte disturbance. Postoperatively, the patient also underwent magnetic resonance imaging which excluded any injury to his spinal cord. The similarity between the case histories presented by Moore et al1 and our patient therefore appears to be evident.
In addition, we think the patient’s follow up is of interest. So far, the patient’s VC has recovered 0.48 l, being 4.2 l and 86% of predicted value in orthostatism. Furthermore, VC now accounts for 2.3 l and 47% of predicted in clinostatism and can assure a normal oxygen saturation during sleep. However, the patient’s diaphragm is still paralysed, since the TwPdi value is extremely low (3 cm H2O) and the fall in VC from orthostatism to clinostatism is significant (45%). The recovery in VC might be due only to the increase in strength of the accessory inspiratory muscles, probably due to the respiratory muscle training courses. This finding further supports the recommendation by Moore et al1 to measure the diaphragm strength separately from global inspiratory muscle strength in patients with raised hemidiaphragms after surgery.
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